• KIPS Transactions on Computer and Communication Systems
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• v.11 no.4
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• pp.127-132
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• 2022

An anonymous encrypted communication networks that make it difficult to identify the trace of a user's access by passing through several virtual computers and/or networks, such as Tor, provides user and data privacy in the process of Internet communications. However, when it comes to abuse for inappropriate purposes, such as sharing of illegal contents, arms trade, etc. through such anonymous encrypted communication networks, it is difficult to detect and take appropriate countermeasures. In this paper, by extending the website fingerprinting technique that can identify access to a specific site even in anonymous encrypted communication, a method for specifying and classifying service types of websites for not only well-known sites but also unknown sites is proposed. This approach can be used to identify hidden sites that can be used for malicious purposes.

• The Journal of the Convergence on Culture Technology
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• v.7 no.4
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• pp.641-652
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• 2021

Drivers have willing to do secondary tasks in situations deemed safe autonomous driving. I studied that positive notifications for secure areas could improve situation awareness and driving performance after TOR(Take over request) in autonomous driving. Comparing TOR alert only and monitoring alert conditions, participants in the positive notification condition showed higher situation awareness and driving performance. Also, in emotional assessment, the positive notification condition showed higher positive evaluation than other conditions. Due to Covid-19, I designed experiments separate online with driving videos in experiment 1 and offline using a driving simulator in experiment 2. This study has implications that presented a different perspective on autonomous driving notification design.

• 한국체육학회지인문사회과학편
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• v.54 no.2
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• pp.431-439
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• 2015

The purpose of this study was to investigate the effects of resistance exercise training and high-protein diet on anabolic factors and insulin resistance of skeletal muscle in sarcopenic obese rats. 50wks of male Sprague-Dawley rats were randomly assigned for 4 groups(Chow, HP, Ex, HPEx) after 6 weeks of high-rat diet induced obesity period. The 8-week of ladder climbing exercise significantly reduced body fat and insulin resistance, significantly increased mTOR activity. However hind limb muscles weight were not changed. When treat with exercise and high-protein diet, body fat and insulin resistance did not improve, but rather the effect of exercise training appeared to be inhibited. Therefore high protein diet for improving the sarcopenic obesity may be need more study about the amount and composition of protein.

• 한국체육학회지인문사회과학편
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• v.55 no.6
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• pp.691-700
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• 2016

The purpose of this study was to investigate the effects of long-term endurance exercise or resistance exercise training on muscle anabolic/catabolic pathway. 50wks-old male Wistar rats(n=30) were randomly assigned for 3 groups (sedentary, endurance exercise, resistance exercise group). After 12-week of training, plantaris muscles were dissect to measure protein level. Akt/mTOR signal-related proteins were significantly increased only after resistance exercise training, but catabolic signal-related proteins, FoxO1 and MuRF1, were significantly decreased after resistance and endurance exercise training. After endurance exercise training, AMPK and PGC-1α protein levels were significantly increased. Therefore, the endurance exercise training has been shown to affect the protein balance of aging muscle through inhibition of muscle protein catabolism. The present results suggest the possibility that not only resistance exercise but also endurance exercise will be affectable to keep or increase muscle volume and capacity of middle-aged people.

• Biomolecules & Therapeutics
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• v.31 no.4
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• pp.402-410
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• 2023

Long-term administration of levodopa (L-DOPA) to patients with Parkinson's disease (PD) commonly results in involuntary dyskinetic movements, as is known for L-DOPA-induced dyskinesia (LID). 5-Hydroxytryptophan (5-HTP) has recently been shown to alleviate LID; however, no biochemical alterations to aberrant excitatory conditions have been revealed yet. In the present study, we aimed to confirm its anti-dyskinetic effect and to discover the unknown molecular mechanisms of action of 5-HTP in LID. We made an LID-induced mouse model through chronic L-DOPA treatment to 6-hydroxydopamine-induced hemi-parkinsonian mice and then administered 5-HTP 60 mg/kg for 15 days orally to LID-induced mice. In addition, we performed behavioral tests and analyzed the histological alterations in the lesioned part of the striatum (ST). Our results showed that 5-HTP significantly suppressed all types of dyskinetic movements (axial, limb, orolingual and locomotive) and its effects were similar to those of amantadine, the only approved drug by Food and Drug Administration. Moreover, 5-HTP did not affect the efficacy of L-DOPA on PD motor manifestations. From a molecular perspective, 5-HTP treatment significantly decreased phosphorylated CREB and ΔFosB expression, commonly known as downstream factors, increased in LID conditions. Furthermore, we found that the effects of 5-HTP were not mediated by dopamine1 receptor (D1)/DARPP32/ERK signaling, but regulated by AKT/mTOR/S6K signaling, which showed different mechanisms with amantadine in the denervated ST. Taken together, 5-HTP alleviates LID by regulating the hyperactivated striatal AKT/mTOR/S6K and CREB/ΔFosB signaling.

• Biomolecules & Therapeutics
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• v.32 no.1
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• pp.162-169
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• 2024

Particulate matter (PM) constitutes a hazardous blend of organic and inorganic particles that poses health risks. Inhalation of fine airborne PM with a diameter of ≤ 2.5 ㎛ (PM_2.5) can lead to significant lung impairments. (+)-afzelechin (AZC), a natural compound sourced from Bergenia ligulata, boasts a range of attributes, including antioxidant, antimicrobial, anticancer, and cardiovascular effects. However, knowledge about the therapeutic potential of AZC for patients with PM_2.5-induced lung injuries remains limited. Thus, in this study, we investigated the protective attributes of AZC against lung damage caused by PM_2.5 exposure. AZC was administered to the mice 30 min after intratracheal instillation of PM_2.5. Various parameters, such as changes in lung tissue wet/dry (W/D) weight ratio, total protein/total cell ratio, lymphocyte counts, levels of inflammatory cytokines in bronchoalveolar lavage fluid (BALF), vascular permeability, and histology, were evaluated in mice exposed to PM_2.5. Data demonstrated that AZC mitigated lung damage, reduced W/D weight ratio, and curbed hyperpermeability induced by PM_2.5 exposure. Furthermore, AZC effectively lowered plasma levels of inflammatory cytokines produced by PM_2.5 exposure. It reduced the total protein concentration in BALF and successfully alleviated PM_2.5-induced lymphocytosis. Additionally, AZC substantially diminished the expression levels of Toll-like receptors 4 (TLR4), MyD88, and autophagy-related proteins LC3 II and Beclin 1. In contrast, it elevated the protein phosphorylation of the mammalian target of rapamycin (mTOR). Consequently, the anti-inflammatory attribute of AZC positions it as a promising therapeutic agent for mitigating PM_2.5-induced lung injuries by modulating the TLR4-MyD88 and mTOR-autophagy pathways.

• Nutrition Research and Practice
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• v.18 no.2
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• pp.210-222
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• 2024

BACKGROUND/OBJECTIVES: Chronic renal failure (CRF) is a complex pathological condition that lacks a cure. Certain Chinese medicines, such as melittin, a major component in bee venom, have shown efficacy in treating CRF patients. On the other hand, the mechanisms underlying the therapeutic effects of melittin are unclear. MATERIALS/METHODS: A 5/6 nephrectomy model (5/6 Nx) of renal failure was established on rats for in vivo assays, and mouse podocyte clone 5 (MPC5) mouse podocyte cells were treated with angiotensin II (AngII) to establish an in vitro podocyte damage model. The 24-h urine protein, serum creatinine, and blood urea nitrogen levels were evaluated after one, 2, and 4 weeks. Hematoxylin and eosin staining, Masson staining, and periodic acid-Schiff staining were used to examine the pathological changes in kidney tissues. A cell counting kit 8 assay was used to assess the cell viability. Reverse transcription polymerase chain reaction and Western blot were used to assess the mRNA and protein levels in the cells, respectively. RESULTS: In the rat 5/6 Nx, melittin reduced the 24-h urinary protein excretion and the serum creatinine and blood urea nitrogen levels. Furthermore, the renal pathology was improved in the melittin-treated 5/6 Nx rats. Melittin promoted podocin, nephrin, Beclin 1, and the LC3II/LC3I ratio and inhibited phosphorylated mammalian target of rapamycin (mTOR)/mTOR in 5/6 Nx-induced rats and AngII-induced MPC5 mouse podocyte cells. Moreover, inhibiting autophagy with 3-MA weakened the effects of melittin on podocin, nephrin, and the LC3II/LC3I ratio in podocytes. CONCLUSION: Melittin may offer protection against kidney injury, probably by regulating podocyte autophagy. These results provide the theoretical basis for applying melittin in CRF therapy.

• Journal of Animal Science and Technology
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• v.54 no.5
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• pp.369-373
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• 2012

AMP-activated protein kinase (AMPK) maintains energy homeostasis in skeletal muscle. Nonetheless, its functional role on protein synthesis with different nutrient availability has not been elucidated. Therefore, the purpose of this study is to examine the effect of AMPK activity on protein content in C2C12 myotubes incubated with low (5 mM; LG) or high (25 mM; HG) glucose media. LG stimulated (p<0.05) AMPK and acetyl CoA carboxylase (ACC) activity compare to those in HG group. Total protein content was higher in myotubes cultured with HG than in those cultured with LG and further increased by AICAR (5-amino-1-${\beta}$-D-ribofuranosyl-imidazole-4-carboxamide). Myotubes cultured with HG showed 7.5% lower UbFL (Ubiquitin Firefly Luciferase)-to-SV40 (Simian virus40) ratio compared to those in LG. Glucose level did not change the phosphorylation level of mammalian target of rapamycin (mTOR). Interestingly, administration of AICAR significantly increased phosphorylation level of mTOR in myotubes cultured with LG but not in those with HG. Overall, this data indicate that AMPK activity and protein turnover are finely regulated in response to different glucose concentration.

• Biomolecules & Therapeutics
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• v.20 no.1
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• pp.43-49
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• 2012

Stimulation of mast cells through the high affinity IgE receptor (Fc${\varepsilon}$RI) induces degranulation, lipid mediator release, and cytokine secretion leading to allergic reactions. Although various signaling pathways have been characterized to be involved in the Fc${\varepsilon}$RI-mediated responses, little is known about the precious mechanism for the expression of tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) in mast cells. Here, we report that rapamycin, a specific inhibitor of mammalian target of rapamycin (mTOR), reduces the expression of TNF-${\alpha}$ in rat basophilic leukemia (RBL-2H3) cells. IgE or specific antigen stimulation of RBL-2H3 cells increases the expression of TNF-${\alpha}$ and activates various signaling molecules including S6K1, Akt and p38 MAPK. Rapamycin specifically inhibits antigeninduced TNF-${\alpha}$ mRNA level, while other kinase inhibitors have no effect on TNF-${\alpha}$ mRNA level. These data indicate that mTOR signaling pathway is the main regulation mechanism for antigen-induced TNF-${\alpha}$ expression. TNF-${\alpha}$ mRNA stability analysis using reporter construct containing TNF-${\alpha}$ adenylate/uridylate-rich elements (AREs) shows that rapamycin destabilizes TNF-${\alpha}$ mRNA via regulating the AU-rich element of TNF-${\alpha}$ mRNA. The antigen-induced activation of S6K1 is inhibited by specific kinase inhibitors including mTOR, PI3K, PKC and $Ca^{2+}$chelator inhibitor, while TNF-${\alpha}$ mRNA level is reduced only by rapamycin treatment. These data suggest that the effects of rapamycin on the expression of TNF-${\alpha}$ mRNA are not mediated by S6K1 but regulated by mTOR. Taken together, our results reveal that mTOR signaling pathway is a novel regulation mechanism for antigen-induced TNF-${\alpha}$ expression in RBL-2H3 cells.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.11
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• pp.4589-4594
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• 2014

The mammalian target of rapamycin (mTOR) signaling pathway is upregulated in the pathogenesis of many cancers, including colorectal cancer (CRC). DEPTOR is an mTOR inhibitor whose expression is negatively regulated by mTOR. However, the role of DEPTOR in the development of CRC is not known. The aim of this study was to investigate the expression of DEPTOR and mTORC1 activity (P-S6) in a subset of CRC patients and determine their relation to tumor differentiation, invasion, nodal metastasis and disease-free survival. Here, Immunohistochemical expression of P-S6 (S235/236) and DEPTOR were evaluated in 1.5 mm tumor cores from 90 CRC patients and in 90 samples of adjacent normal mucosa by tissue microarray. The expression of P-S6 (S235/236) was upregulated in CRC, with the positive rate of P-S6 (S235/236) in CRC (63.3%) significantly higher than that in control tissues (36.7%, 30%) (p<0.05). P-S6 (S235/236) also correlated with high tumor histologic grade (p=0.002), and positive nodal metastasis (p=0.002). In contrast, the expression level of DEPTOR was correlated with low tumor histological grade (p=0.006), and negative nodal metastasis (p=0.001). Interestingly, P-S6 (S235/236) expression showed a significant negative association with the expression of DEPTOR in CRC (p=0.011, R= -0.279). However, upregulation of P-S6 (S235/236) (p=0.693) and downregulation of DEPTOR (p=0.331) in CRC were not significantly associated with overall survival. Thus, we conclude that expression of DEPTOR negatively correlates with mTORC1 activity and tumor progression in CRC. DEPTOR is a potential marker for prognostic evaluation and a target for the treatment of CRC.